Arterial inflammation in patients with HIV.

Abstract

CONTEXTCardiovascular disease is increased in patients with human immunodeficiency virus
(HIV), but the specific mechanisms are unknown.OBJECTIVETo assess arterial wall inflammation in HIV, using 18fluorine-2-deoxy-D-glucose positron
emission tomography (18F-FDG-PET), in relationship to traditional and nontraditional
risk markers, including soluble CD163 (sCD163), a marker of monocyte and macrophage
activation.DESIGN, SETTING, AND PARTICIPANTSA cross-sectional study of 81 participants investigated between November 2009 and
July 2011 at the Massachusetts General Hospital. Twenty-seven participants with HIV
without known cardiac disease underwent cardiac 18F-FDG-PET for assessment of arterial
wall inflammation and coronary computed tomography scanning for coronary artery calcium.
The HIV group was compared with 2 separate non-HIV control groups. One control group
(n = 27) was matched to the HIV group for age, sex, and Framingham risk score (FRS)
and had no known atherosclerotic disease (non-HIV FRS-matched controls). The second
control group (n = 27) was matched on sex and selected based on the presence of known
atherosclerotic disease (non-HIV atherosclerotic controls).MAIN OUTCOME MEASUREArterial inflammation was prospectively determined as the ratio of FDG uptake in the
arterial wall of the ascending aorta to venous background as the target-to-background
ratio (TBR).RESULTSParticipants with HIV demonstrated well-controlled HIV disease (mean [SD] CD4 cell
count, 641 [288] cells/μL; median [interquartile range] HIV-RNA level, <48 [<48 to
<48] copies/mL). All were receiving antiretroviral therapy (mean [SD] duration, 12.3
[4.3] years). The mean FRS was low in both HIV and non-HIV FRS-matched control participants
(6.4; 95% CI, 4.8-8.0 vs 6.6; 95% CI, 4.9-8.2; P = .87). Arterial inflammation in
the aorta (aortic TBR) was higher in the HIV group vs the non-HIV FRS-matched control
group (2.23; 95% CI, 2.07-2.40 vs 1.89; 95% CI, 1.80-1.97; P < .001), but was similar
compared with the non-HIV atherosclerotic control group (2.23; 95% CI, 2.07-2.40 vs
2.13; 95% CI, 2.03-2.23; P = .29). Aortic TBR remained significantly higher in the
HIV group vs the non-HIV FRS-matched control group after adjusting for traditional
cardiovascular risk factors (P = .002) and in stratified analyses among participants
with undetectable viral load, zero calcium, FRS of less than 10, a low-density lipoprotein
cholesterol level of less than 100 mg/dL (<2.59 mmol/L), no statin use, and no smoking
(all P ≤ .01). Aortic TBR was associated with sCD163 level (P = .04) but not with
C-reactive protein (P = .65) or D-dimer (P = .08) among patients with HIV.CONCLUSIONParticipants infected with HIV vs noninfected control participants with similar cardiac
risk factors had signs of increased arterial inflammation, which was associated with
a circulating marker of monocyte and macrophage activation.